At the conclusion of the KPMA annual meeting on March 10, I was left with a deep feeling of gratitude, accomplishment, and pride. We held the meeting at a new venue to attract psychiatrists from multiple areas of the Commonwealth. The enthusiasm and dedication of our presenters and panelists was palpable. Our presenters volunteered their time to educate our membership on the topics of eating disorders, pharmacology, ADHD, neurodivergence, cannabis, and covid-19. In addition to invaluable knowledge that was shared, we were able to reconnect with our colleagues from across the state and experience camaraderie and fellowship. I am grateful for the selfless service of our presenters and panelists, and for the participation and attendance of our members.
I am particularly grateful for the hard work and dedication of Dr. Mark Wright, the outgoing chairperson of the scientific committee. His leadership and guidance is irreplicable, and I hope to rely on his advice, mentorship, and guidance as the incoming chair.
The landscape of mental health care is rapidly evolving in both press and practice. Psychiatric disorders are becoming a topic of discussion nationwide, and interest in novel psychiatric therapies is gaining momentum. As we look into the future, I hope to humbly follow in the footsteps of my predecessor and provide the psychiatrists of Kentucky an avenue for sharing opinions and ideas, and a platform for education on mental health issues that are relevant and of interest to the practicing psychiatrist.
We could not have held this meeting without the tireless efforts of our executive director, Miranda Sloan, who was the glue that held us together and navigated the schedules of our busy physicians. Thank you to our president Dr. Suleman, the scientific committee, and the executive council, for their leadership and dedication to organized psychiatry. I would also like to personally thank each member of KPMA for trusting us with your time, and for your continued involvement in our meeting. I look forward to being of service to you all as we move toward planning our next scientific meeting in 2024.
Please join us on Friday, March 10, 2023, beginning at 8:00am – 5:00pm at the Cardinal Club in Simpsonville, Kentucky. Tickets may be purchased via Eventbrite using the link below. CME pending approval.
Please join us Thursday, November 11th, 2021, virtually for a Town Hall beginning at 6:30pm. Our schedule is as follows:
6:30pm – 7:00pm Sheila Schuster, Ph.D., will discuss assessment thus far from Severe Mental Illness Task Force and tentative recommendations for improving access and care for this patient population.
7:00pm – 7:30pm Gagandeep Kaur, M.D, will discuss rising number of young adolescent suicidality/attempts, particularly in young girls.
7:30pm – 8:00pm Allen Brenzel, M.D, will provide a high level overview of current mental health and SUD/OUD climate in Kentucky. Discuss what strategies/initiative (if any) are being planned at the state level to mitigate for Kentuckians suffering from mental illness/SUD/OUD, with respect to the pandemic.
Registration is free for this virtual event. You may register using the link below. A calendar invite is attached as well.
Our meeting slated for Friday, September 24th, at the Louisville Boat Club has been postponed until the spring. We will announce further plans later this month. If you have already registered, please use the link below to indicate if you prefer a credit or full refund.
Raymond Pary, M.D., VA Hospital, VA Staff Psychiatrist and Steven Lippmann, M.D., Retired PsychiatristLouisville, KY
Schizophrenia has a heterogeneous clinical prodrome and variable outcome. It usually occurs with symptoms of delusions and auditory hallucinations. Sometimes, affective presentations include depression or mania, or less often, catatonia with bradykinesia and mutism. Such presentations are often labeled schizoaffective disorder or catatonia, respectively. Clinical patterns alter over time as do lifetime diagnoses and are unpredictably identified even by accomplished psychiatrists. Agitated and/or violent behavior is occasionally observed.
A historical perspective on schizophrenia starts with Emil Kraepelin. In the early 1900s, he attributed degenerative cells in the brain as being responsible for the deteriorating course of illness. The brain pathology is likely genetic and/or related to gene expression, but there are many unanswered questions about the [RP1] role genes have in the neuropathology. Further understanding is needed to understand how the heterogeneous brain connections and circuits contribute to schizophrenia. Diagnoses, now based on subjective clinical symptoms, will in the future hopefully be determined by documentable brain changes. Some amelioration of clinical severity for many patients followed the 1960s advent of administering antipsychotic medications; yet, responses to these drugs is variable.
Sigmund Freud speculated that schizophrenia resulted from disintegration of the ego and separation from reality. Accordingly, the death of the ego produced a loss of self-identity. Unsuccessful attachment to the opposite sex parent and disordered family patterns were thought to contribute to the psychopathology. Paranoid delusions are stress-induced, based on unconscious homosexual impulses. These theories were further elaborated and included the concept of the “schizophrenogenic mother”. Such concepts might have retarded research progress about neurobiology, and there is a dearth of evidence corroborating that mothers actually cause schizophrenic illnesses in their offspring.
Pneumoencephalographic studies reveal that people with schizophrenia have abnormally large brain ventricles. Computerized tomography corroborates this finding. It also suggests that schizophrenia begins in utero as a neurodevelopmental disorder, and that manifestations vary over the life cycle. Ventricular enlargement is not static and appears to exert influence on the illness pathology.
Magnetic resonance brain imaging research among neonates at high risk for schizophrenia reveals that cortical thickness alterations, diminished gray matter volume, and white matter changes occur in the same regions as where pathology is documented in adults with schizophrenia. This supports a neurodevelopmental abnormality. However, structural investigations document non-specific gray and white matter abnormalities that differ among patients and are not diagnostic.
Positron emission tomography measures blood flow and glucose utilization, depicting abnormalities of brain function. Such investigations evidence deficits in working memory, executive functioning, processing speed, and language production. Imaging studies reveal anatomic abnormalities in the medial frontal cortex, the posterior cingulate cortex, reduced cortical thickness, white matter abnormalities, and enlarged lateral ventricles. The subcortical amygdala, thalamus, hippocampus, and nucleus accumbens are documented to be subnormal in size.
The dopamine hypothesis involving these structures during this illness has undergone refinements over time. In short, the assumption was that hyperactivity of dopamine D2 receptors influence the presence of positive symptoms, while hypofunction of the D1 receptor in the prefrontal cortex may have a role in the negative manifestations of disease. Abnormalities of dopamine may change over different stages of illness and are dependent on other neurochemical systems. These interactive neuronal networks also at least involve glutamate, gamma-aminobutyric acid, and serotonin.
There are progressive alterations in the brains of some patients with schizophrenia. The apparent brain volume changes also might be explained to be imaging artifacts or induced by exposure to antipsychotic pharmaceuticals. The neuropathology leading to hallucinations and delusions remains unexplained. Similar questions apply to the pathological variance among individuals. It is still not established as to whether early detection and treatment mitigate disease progression. Nevertheless, antipsychotic drugs exert a positive influence on the lives of many people with this illness; withdrawing these pharmaceuticals usually yields worsening clinical outcomes for those affected.
Schizophrenia is a disease with genes influencing the development of brain structure and neuronal performance. Alteration of cortical and subcortical structures has pathological consequences for white matter function. These vary between individuals, but abnormalities in neuronal connectivity occurs in many individuals with this illness. Research continues. Antipsychotic medicines generally induce some clinical improvement; yet, there remains no means to cure or fully understand this terrible disease. The neurobiology of schizophrenia is still an enigma. A Suggested ReadingDelisi, L. The Neurobiology of Schizophrenia. Focus 2020; 18 (4): 368-374
